188 
PULMONARY MODELS 
When it became clinically obvious that the 
animals were in a terminal state, they were sac- 
rificed. The thoracic cavity was opened immedi- 
ately and small segments of the heart, lung, and 
liver were taken for electron microscopy. Sec- 
tions were taken of all major organs for light 
microscopic evaluations. Preparation of the tis- 
sue for light microscopic and ultrastructural 
studies were similar to methods previously 
described.^ 
RESULTS 
The average survival time of the infant mon- 
keys was 241 days (199-325). Throughout the 
early stages of the experiment the animals 
showed few outward effects of monocrotaline 
intoxication. There were only slight increases in 
SGOT and serum bilirubin, while A/G ratios of 
the serum and the total serum protein were not 
altered appreciably. Within a month or two 
prior to death, there was an increase in Hct from 
40% to 60% and a concomitant rise in hemoglob- 
in concentration (12 vs. 17 g %). Five animals 
having Hcts in excess of 55% were injected 
with red blood cells tagged with Cr^^ There 
was a 20% increase in the circulating red cell 
volume when compared to that of normal ani- 
mals of similar age. At the time when the mon- 
keys had a decrease in arterial and venous PO2 
(110 vs. 42, and 55 vs. 27 mm Hg, respectively) 
a concomitant increase in arterial pCOo (23 vs. 
42 mm. Hg) was recorded. The pH of the ar- 
terial blood was also decreased in the experi- 
mental animals during this period (7.49 vs. 
7.27). Right ventricular pressures taken on 
these animals exceeded 50 mm Hg as opposed to 
an average of 20 mm Hg in the control animals. 
The pulmonary artery pressures in the control 
monkeys averaged 16 mm Hg, while those of 
the monocrotaline group had values ranging be- 
tween 35 and 45 mm Hg. As the experiment 
progressed, respiratory insufficiency became 
more severe. Prior to death, the least exertion 
produced marked cyanosis, and frequently re- 
quired oxygen therapy to facilitate survival. 
In order to obtain ideal tissues for ultrastruc- 
tural studies, the animals were sacrificed when 
cardiorespiratory dysfunctions reached a stage 
that death was imminent. At the time of 
necropsy, the bodies of all the experimental ani- 
mals were well nourished. The major pathologic 
alterations were located in the heart and the 
lungs ; although pink in color the lungs were 
quite firm and failed to collapse readily on expo- 
sure to atmospheric pressure. There was also 
hypertrophy of the left heart and marked dila- 
tation and hypertrophy of the right heart. The 
right ventricle extended to the apex of the heart 
and the walls were decidedly thickened. The dil- 
atation of the right heart was also exemplified 
by the increase in size of the bicuspid valve 
which averaged 4.5 cm in experimental animals 
and 2.0 cm in the control animals. 
Microscopically, there were extensive 
changes in the respiratory tissue. Partial to 
complete occlusion of the capillaries, arterioles, 
and small muscular arteries throughout the 
lungs was observed (Figure 1). In addition, fib- 
rous thickening of the alveolar septum was 
prominent in the areas closely associated with 
the occluded vessels. Thrombosis and arteritis 
involving the larger arteries were present in 
five experimental animals. 
There was fragmentation, desquamation, and 
dehiscence of the capillary endothelium. These 
aff'ected capillaries invariably were filled with 
platelet and fibrin thrombi. The changes in the 
pulmonary arteries were related to the mor- 
: r. ... 
Figure 1. — Lung section from a monocrotaline intoxi- 
cated animal that survived six and one half months. 
There is a decided thickening of the arterial walls 
primarily due to muscle hypertrophy (arrow). Inter- 
alveolar septa are also increased in thickness as a re- 
sult of increased fibrous connective tissue, fluid and 
cellular components. H & E stain; x 176. 
